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case records of the massachusetts general hospital

The new england journal of

medicine

n engl j med 351;12

www.nejm.org september 16, 2004

1240

Founded by

Richard C. CabotNancy Lee Harris, m.d.,

Editor

Jo-Anne O. Shepard, m.d.

, Associate Editor

Stacey M. Ellender, Assistant Editor

Sally H. Ebeling, Assistant Editor

Christine C. Peters, Assistant Editor

Case 29-2004: A 75-Year-Old Woman with Acute Onset of Chest Pain

Followed by Fever

Adolf W. Karchmer, M.D., David F. Torchiana, M.D.,

Claudia U. Chae, M.D., M.P.H., Nadeem A. Afridi, M.D.,and Stuart L. Houser, M.D.

From the Division of Infectious Diseases,Beth Israel Deaconess Medical Center(A.W.K.); the Divisions of Cardiac Surgery(D.F.T.), and Cardiology (C.U.C., N.A.A.),and the Department of Pathology (S.L.H.),Massachusetts General Hospital; and theDepartments of Surgery (D.F.T.), Medicine(C.U.C., A.W.K., N.A.A.), and Pathology(S.L.H.), Harvard Medical School — all in

Boston.

N Engl J Med 2004;351:1240-8.

Copyright © 2004 Massachusetts Medical Society.

Dr. Claudia U. Chae:

A 75-year-old woman was admitted to the hospital because of chest

pain. One week before admission she had had an illness characterized by fever, head-ache, nausea, malaise, and anorexia. On the night before admission, she awoke witha sensation of heaviness in her chest, dyspnea, and sweating, without nausea, vomit-

ing, palpitations, or syncope. There was no improvement with the administration of sublingual nitroglycerin. She was admitted to the hospital.

The patient had had exertional chest pain for several years, which had been treated

and controlled with sublingual nitroglycerin. Forty months before admission, a cardiacultrasonographic study showed mild aortic stenosis. Eleven months before admission,she had had a non–Q-wave myocardial infarction. Cardiac catheterization revealed65 percent stenosis of the proximal right coronary artery and severe stenosis of a cir-

cumflex obtuse marginal branch; percutaneous transluminal coronary angioplasty wasperformed, with stent placement. A cardiac ultrasonographic examination disclosed

aortic stenosis with a valve area of 1 cm

2

and a mean gradient of 28 mm Hg; the left ven-tricular systolic function was normal. On the day after the placement of the stent, the

patient had episodes of tachycardia associated with dizziness; an electrophysiologicalstudy showed an easily inducible typical atrioventricular nodal tachycardia, and radio-frequency ablation was performed.

The patient had a history of hypothyroidism and in the past had had a transient ce-rebral ischemic attack, which had been managed by performing a left carotid endarter-

ectomy. Her medications were atenolol, lisinopril, fluvastatin, levothyroxine, prometh-azine, and aspirin. She drank alcohol occasionally and had smoked cigarettes in

previous years. Her mother had had diabetes mellitus and heart disease, and her fatherhad died at 67 years of age from a myocardial infarction.

On physical examination, the jugular venous pressure was normal. The tempera-

ture was 37°C, the heart rate 68 beats per minute, and the respiratory rate 16 breaths perminute. The blood pressure was 140/70 mm Hg. The carotid pulses were + bilaterally.

pres en t at i on of cas e

Copyright © 2004 Massachusetts Medical Society. All rights reserved.Downloaded from www.nejm.org on March 27, 2005 . This article is being provided free of charge for use in Indonesia.



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The lungs were clear. A systolic murmur, grade 2

of 6, was heard at the right upper sternal border, ra-diating to both carotid arteries; no pericardial rub was detected. The abdomen was unremarkable.

There was no peripheral edema; the femoral puls-es were + to ++ without bruits, and the pedal pulses

were ++. No focal neurologic deficit was detected.The urine was positive for protein (++), ketones

(+++), and bilirubin (+); the sediment contained50 to 100 white cells, 3 to 5 red cells, and moderate

amounts of bacteria per high-power field. The lev-els of urea nitrogen, creatinine, conjugated and to-tal bilirubin, phosphorus, magnesium, electrolytes,

aspartate aminotransferase, alanine aminotrans-ferase, amylase, lipase, creatine kinase, and crea-

tine kinase MB were all normal. Other laboratory values are shown in Tables 1 and 2.

An electrocardiogram showed a normal rhythmat a rate of 78 beats per minute and right bundle-

branch block with left anterior hemiblock; repeat-ed tracings revealed normal rhythm and right bun-dle-branch block, with ST-segment depression of

0.5 mm inferiorly and as much as 1 mm in leads V

4

through V

6

. A chest radiograph showed cardio-

megaly; the mediastinal contour was within normallimits, and the lungs were clear.

Specimens of blood and urine were obtained

for culture, and levofloxacin was begun as treatment for a possible urinary tract infection. The patient

was treated with aspirin, beta-blockers, nitrates, andmorphine in the emergency room, and her initial

chest pain resolved over the course of four hours.

She had recurrent chest pain on the first hospitalday and two further episodes on the fourth hospital

day; the patient reported that the pain resembledthe angina she had had in the past, and it appeared

to respond to treatment with nitrates. The troponinT level was elevated, at 0.21 ng per milliliter, on ad-

mission; it decreased to 0.17 ng per milliliter onthe next day, was 0.19 ng per milliliter on the fourthhospital day, and then subsequently declined. The

levels of creatine kinase and creatine kinase MB re-mained normal. Minidose heparin was injected for

prophylaxis against deep venous thrombosis.Twelve hours after admission, the temperature

rose to 38.5°C, and a planned cardiac catheteriza-tion was aborted. The temperature rose daily there-after to between 38.4 and 39.3°C, accompanied

by shaking chills. Chest radiographs revealed that the heart and mediastinum were normal; there was

mild atelectasis in the right lower lobe but no evi-dence of pneumonia. On the third hospital day,

computed tomographic (CT) scanning of the ab-

domen and pelvis revealed no abnormalities.On the fifth hospital day, two of the six cultures

of blood drawn on the second hospital day yield-

ed gram-positive cocci in pairs and short chains, which were later identified as Streptococcus anginosus

(

S. milleri

group). Treatment with vancomycin wasbegun. A transthoracic ultrasonographic study dis-

closed valvular aortic stenosis with calcificationof all three leaflets. An echolucent area, 2.3 cm by 0.92 cm, was present anterior to the right coronary

cusp (Fig. 1A and Video Clip 1 in the Supplemen-tary Appendix, available with the full text of this

article at www.nejm.org), and several small mo-bile echodensities on the atrial and ventricular side

Table 1. Hematologic Laboratory Data.

Variable On Admission

Hematocrit (%) 34.4

White-cell count (per mm

3

) 11,400

Platelet count (per mm

3

) 117,000

Mean corpuscular volume (

m

m

3

) 85

Prothrombin time (sec) 13.5

Partial-thromboplastin time Normal

* To convert the value for glucose to millimoles per liter,multiply by 0.05551. To convert the value for calcium tomillimoles per liter, multiply by 0.02495. To convert thevalues for cholesterol to millimoles per liter, multiply by0.02586.

Table 2. Blood Chemical Values.*

Variable On Admission

Glucose (mg/dl) 143

Calcium (mg/dl) 8.1

Cholesterol (mg/dl)

Total 107

High-density lipoprotein 10

Low-density lipoprotein 71

Triglycerides (mg/dl) 129

Protein (g/dl)

Total 5.7

Albumin 1.9

Globulin 3.8

Alkaline phosphatase (U/liter) 201

Lactate dehydrogenase (U/liter) 284

Troponin T (ng/ml) 0.21




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of the cusps were seen (Fig. 1B and Video Clip 2 inthe Supplementary Appendix). The peak transaor-tic gradient was 36 mm Hg and the mean gradient

20 mm Hg. There was moderate aortic regurgita-tion as visualized on Doppler ultrasonography.

There was symmetrical left ventricular hypertro-phy; the size and systolic function of the left ven-

tricular cavity were normal. CT scanning of thebrain revealed no abnormalities. Treatment with in-travenous gentamicin and vancomycin was begun,

and levofloxacin was discontinued.On the sixth hospital day, a transesophageal car-

diac ultrasonographic study disclosed thickeningof the aortic root and a hypoechoic area anterior

to the aortic valve. Mobile, hyperechoic massesconsistent with vegetations were present on theright coronary cusp; the largest measured 0.75 cm

by 0.46 cm and was attached to the right aortic leaf-let (Fig. 1C and Video Clip 3 in the Supplementary

Appendix). No evidence of leaflet perforation orfistula formation was detected. There was Doppler

evidence of moderate aortic regurgitation (Fig. 1Dand Video Clip 4 in the Supplementary Appendix).Left ventricular size and systolic function were nor-

mal. There was a small pericardial effusion with ev-idence of right atrial inversion during a major por-

tion of the cardiac cycle, consistent with elevationof pericardial pressure. Another chest radiograph

Figure 1. Echocardiograms.

A parasternal, long-axis view (Panel A) from the transthoracic echocardiogram shows a lucent area adjacent to the aorticroot, indicating an abscess of 2.3 cm by 0.92 cm (arrows). A color Doppler study (Panel B) shows a jet of aortic regurgi-

tation (yellow-orange) and aortic insufficiency (blue). A transesophageal echocardiographic view of the aortic-valve leaf-lets (Panel C) demonstrates a shaggy thickening consistent with valvular vegetations (arrows). A transesophageal

echocardiogram view of the aortic-valve leaflets as highlighted in a color-flow Doppler study (Panel D) shows evidenceof aortic insufficiency. LA denotes left atrium, Ao aorta, and AoV aortic valve.

A B

C D

Ao

LA

LA

AoV

AoV

AoV

Aov




n engl j med 351;12



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disclosed mild cardiomegaly with clear lungs. Peni-

cillin G was substituted for vancomycin, in responseto results of tests to determine the sensitivity of theorganism. The spiking fevers and chills continued.

The results of cultures of blood from the fifth andsixth hospital days were negative.

On the seventh hospital day, chest radiographsshowed an enlarged cardiac silhouette and bilat-

eral pleural effusions with associated atelectasis.The temperature rose to 39.3°C, with rigor.

Dr. Chae:

This 75-year-old woman with a history of coronary artery disease and aortic stenosis came to

the hospital with chest pain of recent onset. The ini-tial impression of the cardiology team was that she

had unstable angina with a non–Q-wave myocar-dial infarction. As we were about to perform cardiac

catheterization, she had a shaking chill, and feverdeveloped. A chest radiograph showed no evidenceof pneumonia. Our differential diagnosis at this

point included subacute bacterial endocarditis, my-opericarditis, and, possibly, cardiac ischemia due

to increased physiological demand in the context of a febrile illness. On the fifth day, we received areport that two blood cultures were positive for

gram-positive cocci, which were later identified as

S. anginosus

(

S. milleri group). We then became very

concerned about endocarditis, changed her anti-biotic coverage, and obtained cardiac ultrasono-

graphic studies.

May we see the imaging studies?

Dr. Nadeem A. Afridi:

A transthoracic echocar-

diogram obtained in the parasternal long axis re- veals a pericardial effusion and an echolucent space,

consistent with an abscess cavity 2.3 cm by 0.92cm, in the anterior aortic-root wall (Fig. 1A and

Video Clip 1 in the Supplementary Appendix). Theaortic valve is thickened, with an attached substancesuspected to be vegetations. Color Doppler visuali-

zation shows moderate-to-severe aortic regurgita-tion with no flow in the space, suggesting no direct

communication between the abscess cavity and theaortic lumen (Fig. 1B and Video Clip 2 in the Sup-

plementary Appendix).A transesophageal echocardiogram again shows

the echolucent space with a mild pericardial effu-

sion, suggesting a diagnosis of pericarditis in thesetting of endocarditis. The valve leaflets are ragged

and thickened and prolapse slightly into the out-flow tract, affecting the integrity of the valve (Fig.

1C and Video Clip 3 in the Supplementary Appen-

dix) and inducing severe regurgitation (Fig. 1D andVideo Clip 4 in the Supplementary Appendix).

Dr. Chae:

At this point, we knew that the patient

had endocarditis; we believed she was receivingappropriate antibiotic therapy, and the blood cul-

tures became negative. However, the findings onthe transesophageal echocardiogram were highly

worrisome, and on the seventh day, her fever spikedagain, and a chest radiograph showed an enlarged

cardiac silhouette. At this point, I sought urgent consultation from my colleagues in infectious dis-eases and cardiothoracic surgery, who had been in-

volved in the patient’s care since the first echocar-diogram was performed. I would like to invite Dr.

Karchmer to give us his thoughts on further evalu-ation and management of this case.

Dr. Adolf W. Karchmer:

In a case such as this, the

infectious-disease consultant needs to address sev-

eral questions. What is the significance of the or-ganism isolated from the patient’s blood? Does thispatient have endocarditis, and if so, what would

be the optimal antimicrobial therapy? What is themeaning of the persistent fever and the echolucent

area in the upper septum anterior to the right coro-nary cusp? What adjunctive therapy would be indi-cated and why, and when should it begin?

This patient’s blood cultures grew S.

anginosus

,a member of the S.

milleri

group. This is the col-

lective designation for three species, S. intermedius,

S. constellatus,

andS. anginosus.

The organisms in this

group are often a

-hemolytic, but occasionally they

can be b

-hemolytic or nonhemolytic. They are foundamong the flora of the oral cavity and the gastro-

intestinal tract and are associated with abscessesand soft-tissue infections, which are often poly-

microbial, in the abdominal cavity, lower respirato-ry tract, orofacial and sinus area, and skin. In addi-

tion, they can cause hematogenous, monomicrobialabscesses in the brain, liver, spleen, subdural space,and bone, and occasionally endocarditis.

1

Does this patient have endocarditis? The modi-fied Duke criteria

2

require the presence of two ma-

jor criteria or one major and three minor criteria toestablish a definite clinical diagnosis of endocar-

ditis (Table 3). This case illustrates the value of echo-cardiography in making the diagnosis of endocar-ditis. Because neither peripheral manifestations

of endocarditis nor a diastolic murmur indicativeof new aortic regurgitation was detected on physi-

cal examination, it remained unclear until echocar-diography was performed whether the patient had

di fferen t i al di ag n os i s




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S. milleri

bacteremia and a focal extravascular in-fection or endocarditis. The echocardiographicfindings and the positive blood cultures meet ma-

jor criteria. If, for the sake of argument, the type of organism and the degree of bacteremia are not

considered sufficient for a major criterion to be met,the bacteremia would meet a minor criterion. Inthe latter case, the patient’s findings would satisfy

three minor criteria: bacteremia, a predisposingcondition (aortic stenosis), and persistent fever;

the echocardiographic findings would constitutea major criterion. Thus, by the Duke criteria, the

patient had definite endocarditis.

Is S. anginosus

a probable cause of this patient’sendocarditis? Viridans streptococci cause 30 to 50

percent of episodes of native-valve endocardi-tis,

3,4

and the S. milleri

group probably accounts

for 1 to 2 percent of cases overall. A study of infec-tive endocarditis caused by organisms of the S. mil-

leri

group

5

found that in 25 percent of the casesthere were extracardiac suppurative foci of infec-tion, 14 percent had intracardiac abscesses, and 90

percent had valvular regurgitation. These cardiacfindings are similar to those in the patient under

discussion.Organisms of the

S. milleri

group are generally

susceptible to penicillin, but they may be relative-ly penicillin-insensitive (with a minimal inhibitory concentration [MIC] of more than 0.1 µg per milli-

liter).

6,7

All of the organisms in the S. milleri

groupare susceptible to vancomycin. As was done in this

case, I would initiate therapy with vancomycin, es-tablish the MIC of penicillin, and — if the isolate

were susceptible — treat the infection with high-

dose penicillin in the range of 16 to 24 million Udaily. It is reasonable to add gentamicin, an amino-glycoside, to penicillin treatment in an attempt to

enhance the bactericidal activity of penicillin, aslong as the organism is not highly resistant to ami-

noglycosides. If the organism had been relatively resistant to penicillin, treatment with the combina-

tion of penicillin and gentamicin or with vancomy-cin should be considered.

This patient’s fever persisted after three days of adequate therapy. Without complications, the timeto defervescence in cases of endocarditis due to vir-

idans streptococci is usually three days; fever per-sists for more than five days in only 10 percent of

cases, and all patients should be afebrile by day 7.

8

Fever that persists after more than seven days of ap-

propriate antimicrobial therapy has been associ-ated with increased mortality.

8

In the context of persistent fever, there are sev-eral possibilities to consider: extensive intracardi-ac infection (intracardiac abscess accounts for 33

to 46 percent of such infections), embolic com-plications (15 to 20 percent), and drug hypersen-

sitivity (approximately 20 percent). Nosocomialevents, such as catheter-related bacteremia, diar-rhea induced by Clostridium difficile,

or pulmonary

emboli, can cause persistent fever, as can extracar-diac foci of infection, such as splenic abscesses, re-

nal abscesses, and abscesses in other areas that might require drainage or special attention.

9,10

The

latter would be an important consideration in this

patient with S. milleri

endocarditis. We also shouldbe concerned about inadequate therapy, either be-

cause the organism is resistant or because the ini-tial microbiologic data were not accurate.

Abscesses are more common with infection of the aortic valve than with infection of other valves,

and may be associated with new regurgitation, peri-carditis, and conduction abnormalities.

11-14

Con-duction abnormalities were present in this patient

but were preexisting and not progressive; however,the transthoracic echocardiogram showed an ab-

scess. Transesophageal echocardiography is mark-edly more sensitive than transthoracic echocardi-

ography for demonstrating intracardiac abscesses, with sensitivity rates of 87 to 100 percent and 28to 36 percent, respectively.

15,16

The echocardio-

gram revealed a newly dysfunctional aortic valve,continued normal left ventricular function, a peri-

valvular abscess, and a pericardial effusion withright atrial inversion during a substantial portion

* The presence of two major criteria or one major andthree minor criteria are necessary for a definitive clinicaldiagnosis of endocarditis.

Table 3. Modified Duke Criteria for Endocarditis.*

Major criteriaPositive blood cultures for typical organismValvular or endocardial involvementEchocardiographic findings of infective endocarditis

(vegetation, abscess, or new partial dehiscenceof prosthetic valve)

New valvular regurgitation

Minor criteriaPredisposing condition (predisposing heart condi-

tion or injection-drug use)Fever ≥38°CVascular phenomena (arterial emboli, septic in-

farcts) or immunologic phenomena (glomerulo-nephritis, Osler’s nodes, Roth spots, rheumatoidfactor)

Microbiologic evidence (not meeting major criteria)




n engl j med 351;12



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of the cardiac cycle. A chest radiograph suggested

an increase in cardiomegaly or a pericardial effu-sion and bilateral pleural effusions. Taken togeth-er, these findings suggest an urgent need for car-

diac surgery to débride the abscess and restoreaortic-valve function.

Can this surgery be performed during active en-docarditis? Three recent studies show that for pa-

tients with active native-valve or prosthetic-valveendocarditis who were operated on during the

course of antibiotic therapy — often with recent positive cultures of blood or material from the siteof infection — there was relatively low operative

mortality.

17-19

Recurrent endocarditis was infre-quent. The timing of surgical intervention is very

important. It is the patient’s preoperative hemody-namic status that predicts postoperative mortality

rates (not the duration of preoperative antibiotictherapy), and this should be the chief consider-

ation in scheduling surgery. Delaying surgery whenthere is increasing ventricular decompensationmay lead to an increase in the rate of mortality. In-

tracardiac abscesses are rarely cured by antibiotictherapy, particularly in the context of persistent fe-

ver, and delay may allow more tissue destruction by uncontrolled infection. This patient’s abscess couldrupture into the pericardial space or form an in-

tracardiac fistula, or the aortic regurgitation could worsen. Finally, there is risk of an embolic com-

plication.In summary, this patient had intracardiac disease

that would not respond to antimicrobial therapy,

and the responsible organism, the S. milleri

group,can cause infection in other sites, such as the liver

and brain. Although surgery carries a small risk of death and of recurrent endocarditis, at this point

I would recommend urgent cardiac surgical intervention.

Dr. Chae:

I asked Dr. Torchiana to discuss how thedecision was made whether and when to take this

patient to surgery.

Dr. David F. Torchiana:

Most patients with native-

valve endocarditis are treated with antimicrobialtherapy and do not need surgery.

20,21

Surgery ismost clearly indicated when there has been destruc-

tion of tissue by infection and when valvular insuf-ficiency and congestive heart failure develop. Other

possible indications for surgery in endocarditis area resistant organism, persistent sepsis, extension

of infection beyond the valve, and recurrent emboli.

The term “complicated endocarditis” has been usedto differentiate those cases in which one or moreof these criteria are present.

21

This patient had

only modest aortic insufficiency, with little, if any,congestive heart failure. The infecting streptococ-

cal organism was relatively sensitive, but she hadextensive infection into the myocardium and per-

sistent sepsis.With a case of acute endocarditis and valvular

insufficiency, the temptation is to treat with anti-biotics and delay surgery if the patient’s conditioncan be managed safely in the interim. Gaining con-

trol of acute sepsis renders surgery and cardiopul-monary bypass less hazardous. Sterilization of the

field may reduce the risk of recurrent infection, es-pecially if foreign material such as a valve prosthe-

sis will be introduced. A sterilized field will havebetter tissue integrity, particularly if three or four

weeks of antibiotic therapy can be instituted beforesurgery, allowing time for scarring and fibrosis todevelop, which helps the valve sutures to hold.

There are pitfalls in delaying surgery, however,and vigilant follow-up is needed if this strategy is

undertaken. Patients with aortic insufficiency, par-ticularly younger patients, may appear to toleratea severe valve lesion with relatively little evidence of

clinical compromise, but their status may in reality be quite precarious. Recurrent emboli may be diffi-

cult to detect, particularly visceral emboli or centralnervous system emboli in patients who already have

an altered mental status. These issues must be kept

in mind when following a patient with endocardi-tis, and they must be factored into decisions on the

timing of surgery. As a general principle, patients with complicated endocarditis do better with sur-

gery than without it, and delay makes no sense if the patient’s health is deteriorating. In this pa-

tient, because of the extensive myocardial infectionand persistent sepsis, I thought that surgery wasindicated.

Once we decided that this patient would proba-bly require surgery, a decision needed to be made

whether to perform coronary angiography. In thiscase, the patient had two indications for coronary

angiography. The first was known coronary artery disease and a prior coronary intervention. Obvious-ly, the potential for new or progressive occlusive

disease made coronary angiography beneficial insurgical planning. Second, this patient had an aor-

tic-root abscess; knowledge of the relative size andcourse of the coronary arteries can be helpful in

di s cus s i on of m an ag em en t




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planning a complex aortic-root reconstruction. In

the absence of risk factors for coronary disease andin younger patients, echocardiography is sufficient preoperative imaging. The necessity of administer-

ing a contrast agent to an already sick patient andthe risk of causing embolization of aortic-valve

vegetations are relative contraindications to angi-ography. Newer techniques for noninvasive coro-

nary imaging, such as CT or magnetic resonanceangiography, may have a role in management in the

future. In this patient, we opted to do preoperativecoronary angiography, which disclosed a 40 per-cent stenosis of the left main coronary artery and

a 50 percent stenosis of the proximal right coro-nary artery.

The principles of valve surgery in endocarditishave changed relatively little since the first reported

surgery in 1965.

22

Infected tissue should be thor-oughly débrided and cultured. There is no clear ad-

vantage in terms of the risk of recurrent infection with either mechanical or tissue prostheses.

18,23-25

The lack of a need for anticoagulant treatment may

make a tissue prosthesis a safer choice early on incomplicated cases, in sick patients, and in intrave-

nous-drug users in whom noncompliance increas-es the risks associated with warfarin.

The choice of prosthesis for patients with en-

docarditis is based on the same criteria as are usedin the absence of infection. Valves that can be re-

paired should be repaired. When replacement isnecessary, tissue valves are used in older patients

and mechanical prostheses in younger patients. In

cases of complicated infection of the aortic root,such as this, implantation of an aortic homograft

(a nonviable, cryopreserved human aortic root) ap-pears to be associated with better early results and

a lower risk of recurrent infection.

26

Both the pli-ability of the homograft tissue and the fact that the

infected field is radically excluded from the blood-stream in this procedure probably contribute to itssuccess rate in spite of the greater associated tech-

nical complexity.At surgery, we found a large aortic-root abscess

extending from the left main artery around to theorigin of the right coronary artery, with purulent

destruction of part of the interventricular septum.Because of the extent of tissue destruction, we useda homograft for root replacement. The left main

coronary artery was reimplanted. The origin of theright coronary artery was surrounded by inflamma-

tory tissue and induration, which precluded mo-bilization. This vessel was ligated proximally and

bypassed with a saphenous-vein graft. The patient

recovered uneventfully, was discharged on the sixthpostoperative day, and went on to complete a six- week course of intravenous antibiotics. She is alive

and well a year later, with no recurrence of endo-carditis.

Acute bacterial endocarditis due to S. anginosus

(

S.

milleri group), with myocardial abscess.

Dr. Stuart L. Houser:

The trileaflet aortic valve was

thickened and had focal areas of calcification

27

(Fig. 2A). Vegetations were present that contained

fibrin, platelets, neutrophils, and invading coloniesof bacteria, findings that are characteristic of acute

bacterial endocarditis (Fig. 2B). The organisms weregram-positive cocci, consistent with the S. angino-

sus

(

S. milleri group) cultured in the patient’s blood.

This patient’s aortic-root abscess indicated tis-sue destruction by a virulent organism. In a study

cli n i cal di ag n os i s

pat h olog i cal di s cus s i on

Figure 2. Resected Aortic Valve.

An aortic-valve leaflet (Panel A) is thickened and contains

blue areas of dystrophic calcification (hematoxylin and

eosin). There is acute endocarditis (Panel B), with neutro-phils and gram-positive bacteria (Brown–Hopps stain).

A

B




n engl j med 351;12



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of the pathogenesis of abscess formation in infec-

tions by S. milleri

, Wanahita et al.

28

observed that

S. milleri

stimulated neutrophil migration to a less-er extent than other viridans streptococci and than

Staphylococcus aureus

and survived better within hu-man neutrophils.

Dr. Chae

: The patient’s chest pain, positive tro-ponin levels, and electrocardiographic changes on

admission have several possible causes. Because of her known coronary artery disease, she may have

had subendocardial ischemia in the setting of in-creased physiological demand from her infection.Alternatively, if the aortic-root abscess had already

formed, her acute presentation could have beendue to infectious perimyocarditis. There are several

complications of endocarditis that may result incoronary ischemia. Rarely, an aortic-root abscess

can cause coronary-artery compression.

29

The most commonly described complication is septic coro-

nary embolism. This occurs in 22 to 50 percent of cases of endocarditis; whereas the majority (up to65 percent) involve the central nervous system,

other major arterial beds may be involved, includ-

ing the coronary arteries.

30

Septic emboli are morefrequent with mitral-valve infections (25 percent)than with aortic-valve infections (10 percent), and

with other organisms (such as S. aureus

and can-dida species) than with S. milleri

.

30

In streptococ-

cal endocarditis, larger vegetations are more likely to embolize, whereas with staphylococcal or fun-

gal endocarditis, the risk is independent of vege-tation size.

31

Another rare complication is the for-

mation of a mycotic coronary aneurysm with in situthrombosis and embolization,

32

although this typeof aneurysm most commonly involves the intracra-

nial arteries.

30

This case illustrates the need for continued vigi-

lance by clinicians with respect to the diagnosis of endocarditis and its possible complications.

Acute bacterial endocarditis with aortic-root abscess,due to infection by S. anginosus (

S. milleri group).

an at om i cal di ag n os i s

references

1.

Clarridge JE III, Attorri S, Musher DM,Hebert J, Dunbar S. Streptococcus intermedius,Streptococcus constellatus,

and Streptococcus angi-nosus

(“

Streptococcus milleri

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